Aneurysms and Pseudoaneurysms

of the Pulmonary Vasculature

Carlos S. Restrepo, MD, and Aimee P. Carswell, MD

Aneurysms of the pulmonary vasculature may arise from the pulmonary arteries, bronchial
arteries, or pulmonary veins. Their pathophysiology and clinical presentation are variable
depending on the underlying condition, some of which have significant morbidity and
mortality. Consequently, imaging plays a central role in the diagnosis and treatment
planning. This review article presents a classification of the different types of aneurysms
that can affect the pulmonary vasculature and reviews the most common conditions
associated with them and discusses their imaging presentation.
Semin Ultrasound CT MRI 33:552-566 © 2012 Elsevier Inc. All rights reserved.

A neurysms and pseudoaneurysms of the pulmonary vas-

culature are rare and most often affect the pulmonary
arteries, but aneurysmal dilation can also involve the sys-
temic bronchial arteries or the pulmonary veins. An aneu-
rysm is commonly defined as a 50% or greater localized
increase in diameter of the affected vessel compared with
adjacent vascular segment. On computed tomography (CT),
the mean main pulmonary artery diameter in the normal
adult is 25 mm ⫾ 3 mm, with 29 mm commonly cited as
the upper limit of normal.1 Normal reference value for the
right and left pulmonary arteries is 20 mm.2,3 In patients
with cardiopulmonary disease, diameters exceeding these
values are considered to be enlarged and are commonly
associated with pulmonary hypertension.4 By this criteria,
diameter ⬎4.5 cm for the pulmonary trunk and 3 cm for
the right or left pulmonary arteries should be considered
aneurysms.
True aneurysms typically involve all 3 layers of the vessel
wall, in contradistinction to a false aneurysm (pseudoaneu-
rysm), which actually represents a contained rupture in
which not all layers of the affected wall are involved. Numer-
ous conditions, both congenital and acquired, can manifest
with pulmonary artery aneurysm (PAA) (Table 1). Overall,
they are rare, although in some of the diseases, aneurysmal
vascular dilation can be one of the most salient imaging man-
ifestations. In the preantibiotic era, 2 infectious diseases, tu-
Division of Thoracic and Cardiovascular Radiology, Department of Radiol-
ogy, The University of Texas Health Science Center at San Antonio, San
Antonio, TX.
Address reprint requests to Carlos S. Restrepo, MD, Division of Thoracic
and Cardiovascular Radiology, Department of Radiology, The Uni-
versity of Texas Health Science Center, 3323 Ivory Creek, San Anto-
nio, TX 78258. E-mail: crestr@gmail.com
berculosis (TB) and syphilis, were responsible for the major-
ity of PAA. Although both are infectious in etiology, the
mechanism and morphological manifestation are entirely dif-
ferent, with syphilis affecting the large pulmonary arteries
and TB affecting smaller intraparenchymal vessels.5 In the
postantibiotic era, other conditions have replaced infection
as the leading cause of PAA, with different disease mecha-
nisms and imaging presentations. The 3 most common
causes for pulmonary artery pseudoaneurysms are infection,
trauma, and malignancy. In 1988, a simple classification pro-
posed by Bartter et al5 divides pulmonary aneurysms into 2
large groups depending on the presence or absence of arte-
riovenous communication and suggests the denomination of
PAA for those without such communication and pulmonary
arteriovenous aneurysms for those in which an arteriovenous
communication is present. Another way of classifying pul-
monary aneurysms is based on the anatomic structure in-
volved, whether it is located in a proximal or distal pulmo-
nary artery or in a pulmonary vein. PAA may also be classified
by etiology or underlying condition.
Aneurysms of the pulmonary trunk, main pulmonary ar-
teries, and their lobar branches are rare. The overall inci-
dence of PAA is unknown, and most articles cite data from an
old large autopsy series, including more than 100,000 autopsies
in which only 8 case of PAAs were found (prevalence of 1 in
14,000).6 The incidence is significantly higher (1.25%) in pa-
tients with severe pulmonary hypertension of any cause and
even higher in patients with Eisenmenger syndrome from an
intracardiac shunt (6%).7,8 Part of the confusion may be related
to the lack of standardized criteria and nomenclature to refer to
dilation and prominence of the pulmonary arteries.
In this article, the pathophysiology and imaging manifes-
tations of the different conditions that can present with pul-
monary aneurysms will be reviewed.

552 0887-2171/$-see front matter © 2012 Elsevier Inc. All rights reserved.
http://dx.doi.org/10.1053/j.sult.2012.04.001
Aneurysms and pseudoaneurysms of the pulmonary vasculature 553

Table 1 Classification of Aneurysms and Pseudoaneurysms of monary hypertension with reversed shunt (right-to-left or
the Pulmonary Vasculature bidirectional shunting), irrespective of the anatomic location
Pulmonary Artery Aneurysms of the original left-to-right central shunt. Among the different
1. Congenital type of intracardiac shunts, patent ductus arteriosus and
a. Valvular/postvalvular stenosis atrial septal defect are the most commonly associated with
b. Increased pulmonary flow (left-to-right shunt), PAA.10 Pathology examination of PAA commonly reveals cys-
Eisenmenger syndrome tic medial necrosis of the arterial wall. Light microscopy and
c. Connective tissue abnormalities (Marfan disease, electron microscopy have also demonstrated a variable de-
Ehler–Danlos disease, Williams–Beuren syndrome, gree of fragmentation of the elastic fibers, increased content
tuberous sclerosis)
of ground substance of the arterial wall, as well as smooth
2. Acquired
a. Pulmonary arterial hypertension
muscle fiber loss.11 In fatal cases, pulmonary artery rupture
b. Cystic medial necrosis with or without dissection is commonly found. Similar to
c. Vasculitis: Behçet disease, Hughes–Stovin aneurysms in other vessels, PAA may be saccular or fusiform,
syndrome, Takayasu arteritis with saccular type more commonly associated with sponta-
d. Infection: tuberculosis (Rasmussen aneurysm), neous rupture.12
pyogenic, fungal, syphilis, schistosomiasis Clinical presentation differs depending on the underlying
e. Endocarditis condition, but chest pain and dyspnea are common manifes-
f. Neoplasms tations. PAAs are considered to be an unstable and life-threat-
g. Trauma ening condition with significant mortality, requiring prompt
h. Iatrogenic diagnosis and treatment. Complications associated with PAA
1. Idiopatic
include in situ thrombosis, pulmonary embolism, dissection,
Bronchial Artery Aneurysm
a. Congenital (sequestration, pulmonary agenesis)
rupture, and extrinsic compression of adjacent struc-
b. Atherosclerosis tures.12-16 Rupture risk is closely related to size and pressure.
c. Vasculitis (Behçet disease, Hughes-Stovin syndrome) According to Laplace’s Law, which describes the changes in
d. Bronchiectasis blood vessel wall tension, radius and thickness associated
e. Tuberculosis and atypical mycobacteria with transfer of intramural energy, the arterial wall tension
f. Sarcoidosis (T) is proportional to the pressure (P) multiplied by the ra-
g. Post-traumatic dius (R) of the affected vessel and is inversely related to the
h. Hereditary hemorrhagic telangiectasis (Osler–Weber– thickness (t) of the arterial wall:
Rendu disease) T ⫽ P ⫻ R/t
i. Idiopathic Therefore, as the diameter increases, so increases the wall
Pulmonary Vein Aneurysm
tension, as well as the risk for rupture. Similarly, increased
1. Isolated (“varix”)
2. Associated with arteriovenous malformation (hereditary
pressure, as is the case with PAH, aggravates the arterial wall
hemorrhagic telangiectasia)
3. Mitral valve disease

Pulmonary Hypertension
Numerous conditions have been reported associated with
PAA, but, probably, the most common underlying factor to
many of them is the presence of pulmonary arterial hyper-
tension (PAH) of any cause. Congenital deficiencies of the
vessel wall, valvular and supravalvular stenosis, and in-
creased flow secondary to left-to-right shunt are common
factors. Hypoplastic pulmonic valve and bicuspid pulmonic
valve have also been implicated. Left-to-right shunt (eg, atrial
septal defect, ventricular septal defect, and patent ductus
arteriosus) resulting in increased volume and pressure over-
load may lead to pulmonary hypertension and aneurysm for-
mation.
In 1897, Dr. Victor Eisenmenger9 reported a case of a
young adult with history of cyanosis since infancy who died Figure 1 Eisenmenger syndrome secondary to a large atrial septal
after massive hemoptysis, with autopsy revealing a large ven- defect in a 40-year-old female. Anteroposterior view of the chest
tricular septal defect, right ventricular hypertrophy, and pul- demonstrates severe pulmonary hypertension with a prominent
monary arterial thrombosis. It was later that Wood8 proposed pulmonary trunk and significant dilation of the central pulmonary
the term Eisenmenger syndrome to refer to all cases of pul- arteries.
554
tension, also increasing the risk of rupture. A common his-
tological finding in the wall of these dilated pulmonary arter-
ies is cystic medial necrosis.12,13 Patients with severe PAH
from Eisenmenger syndrome present higher risk of rupture
and dissection than other causes of PAH.
The predominant imaging finding in patients with PAA
secondary to pulmonary hypertension is the presence of sig-
nificantly enlarged central pulmonary arteries with rapid ta-
pering of the more peripheral vasculature (Fig. 1). The pul-
monary trunk may be severely dilated, creating a rounded
mass-like mediastinal opacity out of proportion to the hilar
pulmonary vessels (Fig. 2). The right and left pulmonary
Figure 2 Severe pulmonary hypertension with aneurysmal dilation
of the pulmonary arteries. (A) Anteroposterior view of the chest
shows aneurysmal dilation of the pulmonary trunk (arrow) and
large bilateral pulmonary arteries. (B) Contrast-enhanced computed
tomography (CT) shows abnormal pulmonary artery dilation with
wall thickening secondary to laminar thrombus (arrow).
C.S. Restrepo and A.P. Carswell
Figure 3 Pulmonary artery aneurysm (PAA) in a 53-year-old male
with pulmonary hypertension. Contrast-enhanced CT of the chest.
(A) Axial image and (B) sagittal reformation show the severely di-
lated pulmonary artery, which is more than 3 times the diameter of
the aorta.
arteries and interlobar pulmonary arteries may be enlarged as
well (Fig. 3). In Eisenmenger patients, laminated thrombus
can develop within the dilated central pulmonary arteries
(70%), as well as in situ thrombosis in more distal pulmonary
arteries (40%) (Fig. 4). In one-fourth of these patients, calci-
fication may develop either in the wall of the dilated artery or
embedded within the mural thrombus.17,18 The magnitude of
the intrapulmonary arterial thrombosis can be so extensive
that the entire right or left pulmonary artery may be oc-
cluded.19 Extrinsic compression of the coronary arteries by a
dilated pulmonary trunk in patients with an intracardiac
shunt has been described.20 Severely dilated pulmonary ar-
teries may also produce bronchial compression and atelecta-
sis. PAA may also arise as a postoperative complication in
patients with surgical correction of congenital heart disease
(Figs 5 and 6).
Aneurysms and pseudoaneurysms of the pulmonary vasculature 555

and 45° north, in particular certain regions of the Far East,

the Middle East, and the Mediterranean region. Vasculitis,
which can affect small, medium, or large caliber veins or
arteries, is a major cause of morbidity and mortality in BD.
Pulmonary vasculitis (arteritis or venulitis) may result in
thrombosis, infarction, hemorrhage, aneurysm, or arterio-
venous fistula. Aneurysms are relatively common in patients
with BD, but the exact prevalence is not well known. In a
large BD outpatient center with more than 2000 patients,
1.1% patients were diagnosed as having PAA.26 Conversely,
in a large retrospective cumulative analysis, including more
than 500 cases, all with pulmonary involvement, one-third
presented PAA.27 The latter probably represents a selection
bias because only cases with pulmonary disease were in-
cluded. PAA in BD is associated with poor prognosis with
30%-50% mortality within 2 years and is one of the leading
causes of death in these patients.25,26 Nearly all patients with
PAA have a history of hemoptysis. Chest pain, dyspnea, and
cough are other less common respiratory complaints.27
BD PAA can be single or multiple, but multiple aneurysms
in a bilateral distribution are the most characteristic presen-
tation. The most common locations are the right lower lobe
and the right and left main pulmonary arteries with a wide

Figure 4 Severe pulmonary hypertension secondary to a large PDA.

(A and B) Cardiac-gated CT of the chest, axial images at two differ-
ent contiguous levels show PAA with mural thrombus (black ar-
rows).

Vasculitis
Two types of vasculitis have commonly been associated with
PAA: Behçet disease (BD) and Hughes–Stovin syndrome
(HSS). Takayasu arteritis can also involve the pulmonary ar-
teries; however, more commonly, it produces pulmonary ar-
tery narrowing and occlusion rather than dilation.21,22 In pa-
tients with Takayasu arteritis with extensive damage to the
pulmonary vascular bed who develop PAH, pulmonary ar-
tery dilation and aneurysm may occur.23,24
BD is a multisystem inflammatory disorder characterized
by vasculitis (5%-30%) that typically affects men between 20
and 30 years of age. It is clinically manifested by the triad of
uveitis (30%-70%) and recurrent ulcers of the oral mucosa
(96%-100%) and genitalia (65%-90%). Other common man- Figure 5 PAA in a 25-year-old male with history of remote surgery
ifestations include skin involvement (25%-80%), positive for congenital transposition of the great arteries. Contrast-enhanced
skin pathergy test, which is pustule formation after skin prick CT (A) axial and (B) coronal maximum intensity projection images.
(10%-50%), and arthritis/arthralgia (30%-80%).25 The high- There is a large pulmonary artery saccular aneurysm in the antero-
est prevalence of BD occurs in geographic areas between 30 lateral right hemithorax (arrows).
556 C.S. Restrepo and A.P. Carswell

(effusion), mediastinum (mediastinitis, pericardial effusion),

and vascular structures (vasculitis, thrombosis, aneu-
rysms).31 BD patients with vascular pulmonary involvement
should be evaluated for intra-abdominal disease because an-
eurysm and occlusion of the abdominal aorta are more com-
mon complications (Fig. 10).30
HSS is another rare form of vasculitis that can be associated
with intrapulmonary aneurysms, also affecting young adult
males. Some consider HSS as a variant or incomplete form of
BD, with the inflammatory vascular component but lacking
some of the other clinical manifestations like oral and genital
ulceration, skin lesions, and uveitis.32 Regardless, these 2
conditions have in common this aneurysm-thrombosis com-
bination. The characteristic clinical features of HSS include
thrombophlebitis, thromboembolism, and multiple pulmo-
nary or bronchial artery aneurysms (BAAs) (Fig. 11). Aneu-
rysms at other anatomic locations (ie, iliac, femoral, popliteal,
carotid and hepatic arteries) have also been described. On
contrast-enhanced CT, the affected pulmonary vessel may
have a normal wall thickness or may show a rim of enhance-
ment consistent with inflammation, with variable degree of
intraluminal filling defect from embolic material or from in
situ thrombosis, features that help to differentiate from
chronic thromboembolism with secondary pulmonary artery
dilation.33-35 Peripheral venous thrombosis may affect cere-
bral venous sinuses, vena cavae, hepatic veins, jugular veins,
iliac veins, femoral veins, or even the cardiac chambers.36

Connective Tissue Abnormalities

Figure 6 PAA in a 21-year-old female with history of surgically re- Aneurysmal dilation of the pulmonary arteries associated
paired Tetralogy of Fallot. Cardiac-gated CT angiography. (A) Axial with soft tissue disorders is much less common than aneu-
image and (B) sagittal reconstruction. There is a chronic saccular
rysm of the aorta and systemic arteries. Pulmonary artery
aneurysm on the anterior wall of the pulmonary trunk with erosion
of the posterior wall of the sternum (arrows). An irregular calcifica-
dilation can be seen in as much as 75% of patients affected by
tion is noted more distally in the pulmonary artery.

size range, fluctuating between 1 and 7 cm in diameter. The

most common imaging finding on chest radiograph is a bi-
lateral or unilateral parahilar nodular or mass-like opacity
(33%-83%) (Fig. 7). Rarely, the nodular opacity may be lo-
cated in the periphery of the lung (4%) or be large enough to
extend to the pleural surface (Fig. 8).26-29 Associated atelec-
tasis, pulmonary infarct, or hemorrhage may manifest as
wedge-shaped, linear, rounded, or irregular opacities. On
contrast-enhanced CT, PAA appears as contrast-enhanced
fusiform or saccular vascular dilations, which commonly
present with variable degree of intraluminal thrombus (Fig.
9). Concomitant involvement of the venous system with su-
perior vena cava or innominate vein occlusion or aneurysmal
dilation may also be present. Collateral circulation may be
prominent with enlarged bronchial arteries in the mediasti-
num.30 Arteriovenous shunts with convoluted vessels have
also been reported. Although conventional chest radiograph
is often the initial imaging tool, CT is the imaging modality of
choice given its capability of providing comprehensive eval- Figure 7 Behçet disease (BD) in an adult male. Chest x-ray demon-
uation of the entire spectrum of thoracic complications af- strates multiple bilateral PAAs in the central parahilar regions (ar-
fecting the lung (hemorrhage, infarction, atelectasis), pleura rows).
Aneurysms and pseudoaneurysms of the pulmonary vasculature
Figure 8 BD in an 18-year-old male with giant PAA (arrows). (A) Conven-
tional chest radiograph shows a left side large rounded opacity. (B) Con-
trast-enhanced CT reveals the enhancing left-sided saccular lesion. (C) Se-
lective catheter angiography confirms the giant left PA aneurysm.
557
Figure 9 BD in a 29-year-old male with history of superior vena cava
thrombosis. Contrast-enhanced CT reveals a partially thrombosed
right lung pulmonary aneurysm (arrow).
Marfan syndrome, both at the level of the aortic root as well as
at the level of the pulmonary artery bifurcation (Fig. 12).37
Even though frank PAA in Marfan have been reported, in-
cluding multiple pulmonary aneurysm in the same patient,
this is an uncommon finding in this condition.38-40 Vascular
Ehler–Danlos syndrome (EDS), formerly known as EDS type
IV, is a rare hereditary connective tissue disorder with tissue
Figure 10 Hughes–Stovin syndrome (HSS) in a 20-year-old male.
Magnetic resonance angiography shows an aneurysm of the distal
aorta (thick arrow) in addition to multiple bilateral pulmonary an-
eurysms (thin arrows).
558
Figure 11 HSS. A 20-year-old male with iliac thrombophlebitis, mul-
tiple PAAs (arrows), and pulmonary hemorrhage. (A) Contrast-en-
hanced CT axial images with mediastinal window depict bilateral
PAAs. (B) Lung window axial image shows diffuse alveolar hemor-
rhage. (C) Magnetic resonance angiography confirms multiple bi-
lateral pulmonary aneurysms (arrows).
fragility predisposing to arterial dilation and rupture. The
most commonly affected vascular segments in decreasing or-
der of frequency are the abdominal visceral arteries, iliac
arteries, aorta, lower extremities, carotid, vertebral, subcla-
vian, pulmonary, and cerebral arteries. In a series of 28 pa-
tients, pulmonary dilation was found in 7% of affected cases.
Thoracic complications include pulmonary hemorrhage and
C.S. Restrepo and A.P. Carswell
hemothorax.41 Dilatation of the pulmonary artery and annu-
lus have also been reported in other types of EDS.42 An asso-
ciation between tuberous sclerosis and PAA has been re-
ported. Smooth muscle proliferation with hamartomatous
transformation of the pulmonary artery may produce elastic
fiber fragmentation, which may end in the development of
PAA.43 Spontaneous PAA and rupture has also been de-
scribed as a rare complication of pulmonary artery stenosis in
a patient with mutation of the elastin gene (William–Beuren
syndrome or Williams syndrome).44
Infection
Both true and false aneurysms can develop as infectious or
mycotic aneurysms of the lung. Aggressive and virulent or-
ganisms (ie, staphylococcus) produce tissue necrosis and de-
struction involving all layers of the arterial wall, resulting in
the formation of pseudoaneurysms, whereas indolent organ-
isms more often cause true aneurysms, in which the arterial
wall is less severely damaged (ie, syphilis). The 3 main patho-
genic mechanisms responsible for the formation of mycotic
aneurysms are bacteremia, resulting in embolization of the
vasa vasorum, blockage of the vascular lumen by septic em-
boli and erosion of the vessel wall by an adjacent pulmonary
infection either by direct extension or through lymphatic
spread.
Pyogenic bacteria (Staphylococcus species, Streptococcus,
Klebsiella, Actinomyces), mycobacteria (TB, atypical mycobac-
teria), syphilis (Treponema pallidum), and several different
fungi (Aspergillus, Candida albicans, coccidioidomycosis) can
cause PAAs and pseudoaneurysms.45,46
Risk factors include bacterial endocarditis (in particular
right-sided infection), intravascular catheters and devices,
immunosuppression, diabetes, pneumonia, long-term ste-
roid therapy, pulmonary hypertension, and extra pulmonary
Figure 12 Marfan syndrome. Contrast-enhanced CT shows dilated
pulmonary artery (4.3 cm) with thickening of the ascending aorta
and surgical graft in the descending aorta in this patient with history
of aortic dissection. (Color version of figure is available online.)
Aneurysms and pseudoaneurysms of the pulmonary vasculature 559

(MDCT) allows the correct identification of bleeding source

by differentiating between aneurysm/pseudoaneurysm of the
pulmonary artery and hypertrophy of the bronchial arteries,
and MDCT should be the imaging modality of choice in
patients with massive hemoptysis being considered for em-
bolization.48 CT may also demonstrate pseudoaneurysms
that were not detected on the main pulmonary artery angio-
gram.49
Rasmussen aneurysm is the name given to PAA associ-
ated with pulmonary TB. Fritz Valdemar Rasmussen50, a
Danish physician, was the first to describe the intimate
relationship between a pulmonary artery and the wall of a
pulmonary cavity in 11 patients with TB and hemoptysis.
In a large autopsy series, the prevalence of Rasmussen
aneurysm in chronic pulmonary TB was 4%, and was as-
sociated with significant mortality from massive bleed-
ing.51 A common misconception is to consider hemoptysis
in pulmonary TB as commonly associated with Rasmussen

Figure 13 Mycotic pulmonary aneurysm in a 67-year-old female

with enterococcus bacterial endocarditis. (A) Contrast-enhanced
axial CT image. There is an infectious aneurysm of the right lower
lobe pulmonary artery (arrow), with an additional cavitary lung
lesion more anteriorly located. (B) Right pulmonary artery selective
catheter angiography. The right lower lobe PAA is nicely depicted
(arrow).

infection. Massive hemoptysis (with a mortality rate that ex-

ceeds 50%) is the most serious complication of a ruptured
pulmonary artery pseudoaneurysm, like those associated
with pulmonary infection.47 In the acute stage, the imaging
appearance of mycotic pulmonary aneurysms may be indis-
tinguishable from those of a neoplastic condition. On con-
trast-enhanced CT, there is an enhancing nodule commonly Figure 14 Mycotic pulmonary aneurysm in a 26-year-old male with
associated with a necrotizing pneumonia or lung cavity. In history of intravenous drug abuse. Contrast-enhanced CT (A) axial
the subacute and chronic stage, the surrounding pneumonia image and (B) volume-rendered 3-dimensional reconstruction.
may have resolved, leaving the dilated vessel as the predom- There is aneurysmal dilation of the left lower lobe pulmonary artery
inant imaging finding (Figs 13 and 14). Multidetector CT (arrows). (Color version of figure is available online.)
560
Figure 15 Rasmussen aneurysm in 62-year-old male with proven
active pulmonary tuberculosis who presented with hemoptysis.
Contrast-enhanced CT, (A) axial and (B) coronal reformation. There
is an irregular opacity with cavitation in the right upper lobe with an
enhancing oval mural sac (arrow). (C) Selective right upper lobe
catheter angiography injection confirms a PAA.
aneurysm. Today, it is well established that the most com-
mon source of hemoptysis in these patients is from the
systemic bronchial circulation and not from the pulmo-
nary vasculature.52 Rasmussen aneurysms can vary in size
and number but most commonly present as a small (⬍1
C.S. Restrepo and A.P. Carswell
cm) single lesion surrounded by a parenchymal opacity,
consolidation, or in the wall of a lung cavity (Fig. 15).53,54
Multiple aneurysms in the same patient, and occasionally
giant aneurysms, may occur.55,56
Malignancy
Pulmonary pseudoaneurysms associated with lung cancer
are rare, and the majority of pulmonary pseudoaneurysms
are secondary to squamous cell carcinoma, in patients who
typically present with massive hemoptysis. Direct tumoral
invasion and erosion of the arterial wall results in arterial
rupture, that when contained will manifest as a pseudoan-
eurysm. Noncontained rupture with massive bleeding if
left untreated is associated with high mortality.57-62 On
contrast-enhanced CT, the imaging findings are those of a
parenchymal opacity or lung mass containing a rounded
hyper vascular lesion usually on the more medial or para-
hilar aspect (Fig. 16). Large necrotizing lung tumors with
pseudoaneurysms and ipsilateral pleural effusion should
raise the possibility of hemothorax from aneurysmal rup-
ture (Fig. 17). Occasionally, primary and metastatic pul-
monary sarcomas may also present as a pulmonary artery
pseudoaneurysm.63-65
Trauma
Penetrating and nonpenetrating trauma may result in pulmo-
nary artery or vein pseudoaneurysm when there is tear or
disruption of all layers of the vessel wall with the extravasated
blood contained by clot and extravascular tissue.66 Despite
the large number of patients with chest trauma, posttrau-
matic pulmonary pseudoaneurysms are uncommon even af-
ter penetrating lung injury. In a series of 22 patients with
penetrating lung injury, 15 of them with gunshot wounds
and 8 with stab wounds who received routine pulmonary
catheter angiography, not one single vascular injury was
Figure 16 Right upper lobe squamous cell carcinoma with pseudo-
aneurysm in a 52-year-old male with hemoptysis. Contrast-en-
hanced CT, axial image. An irregular and spiculated right upper
lobe mass contains a hypervascular internal collection of contrast
consistent with a pseudoaneurysm (arrow).
Aneurysms and pseudoaneurysms of the pulmonary vasculature 561

and hemoptysis should suggest the diagnosis.72 In hemodynam-

ically stable patients, contrast-enhanced CT is the imaging mo-
dality of choice, revealing the variable in shape and size-enhanc-
ing lesion, usually similar in density to the adjacent pulmonary
vasculature, or, in case of central pulmonary artery injury, irreg-

Figure 17 Pulmonary pseudoaneurysm secondary to squamous cell

lung cancer in a 53-year-old male. Contrast-enhanced CT of the
chest. (A) Axial image shows a large necrotic tumor with diffuse
opacification of the right lung, with an enhancing pseudoaneurysm
in the infrahilar region (arrow). (B) Sagittal reconstruction shows
the aneurysmal sac (arrow) surrounded by the diffuse parenchymal
opacity and necrotic tissue.

found.67 The low incidence of this complication of thoracic

trauma may be related to the low pressure of the pulmonary
artery. Nevertheless, rupture and massive hemoptysis with sig-
nificant mortality have been documented in numerous
cases.68,69 In the acute stage, pulmonary hemorrhage is appreci-
ated surrounding the pseudoaneurysm, commonly associated
with pleural fluid (Figs 18 and 19). In those rare cases with late
presentation, the surrounding lung may be normal or, depend-
Figure 18 Traumatic pseudoaneurysm (arrows) of the left lung in a
ing on the size, may exhibit compressive atelectasis.70,71 Chest 28-year-old female patient with gunshot wound. (A) Contrast-en-
radiographs may demonstrate nonspecific consolidation that hanced CT of the chest, axial image depicts a pulmonary pseudo-
during the following days may evolve into a lung nodule or aneurysm in the left hilar region. (B) Coronal reformation shows the
mass. Similar to other types of pseudoaneurysms, hemoptysis is aneurysmal sac superior and lateral to the left ventricle. (C) Catheter
the most common clinical manifestation. Therefore, in the set- angiography with left pulmonary artery injection confirms the com-
ting of trauma, the combination of radiographic abnormalities munication of the aneurysm with the left pulmonary artery.
562
Figure 19 Pulmonary artery pseudoaneurysm secondary to blunt
thoracic trauma in a motor vehicle accident. Contrast-enhanced CT
shows the irregularity of the right pulmonary artery with an intimal
tear flap (arrow). Large bilateral hemothoraces are also noted.
Figure 20 Traumatic pulmonary artery pseudoaneurysm. (A) Con-
trast-enhanced CT axial image. There is a left pulmonary artery
pseudoaneurysm (arrow), with a mediastinal hematoma. (B) Cath-
eter angiography with left pulmonary artery selective injection. The
irregular false aneurysm on the proximal left pulmonary artery is
confirmed (arrow).
C.S. Restrepo and A.P. Carswell
Figure 21 Postlung biopsy pulmonary pseudoaneurysm in a 75-
year-old patient presenting with massive hemoptysis. Contrast-en-
hanced CT, axial image shows a large pseudoaneurysm lateral to the
left pulmonary artery (arrow), surrounded by fluid and parenchy-
mal consolidation.
ular contour of the arterial wall and mediastinal hematoma (Fig.
20).73,74
Iatrogenic
Iatrogenic perforation of a pulmonary artery may also result
from the use of flow-directed pulmonary artery catheters
(also called Swan–Ganz catheters), widely used in the criti-
cally ill patients. Complications are rare but may result in
pulmonary hemorrhage, thrombosis, pseudoaneurysm, pul-
monary infarction, and death. Pulmonary artery rupture oc-
curs in 0.03%-0.5% of patients, with a mortality rate as high
as 70%.75 Contained rupture results in a pseudoaneurysm,
which occurs in 0.16% of the cases.76 This complication
should be suspected in patients with persistent peripheral
location of the catheter who develop a new opacity in the
vicinity of the balloon. Contrast-enhanced CT confirms the
diagnosis.77 Traumatic lung injury from thoracostomy tube
placement, lung biopsies, radiofrequency ablation of lung
tumor, and pulmonary surgery are other rare causes of iatro-
genic pulmonary pseudoaneurysms (Fig. 21).78-80
Bronchial Artery Aneurysms
BAAs may be mediastinal or intrapulmonary in location. Dif-
ferent congenital and acquired medical conditions are asso-
ciated with BAA. Pulmonary TB and atypical mycobacterial
infection are some of the most common causes of BAA, par-
Aneurysms and pseudoaneurysms of the pulmonary vasculature 563

ticularly in developing countries. They are reported in about

1% of all selective bronchial arteriograms and in 7% of pa-
tients with TB presenting with hemoptysis.52,81 Other causes
of BAA include bronchiectasis, pulmonary sequestration,
pulmonary agenesis, sarcoidosis, silicosis, vasculitis (BD,
HSS), trauma, atherosclerotic disease, and arteriovenous
malformation (AVM). Besides hemoptysis, which is the most
common clinical manifestation, BAA may present clinically
by spontaneous mediastinal hematoma, mass effect on the
airways or the esophagus.33,82,83 BAA varies in size from a few
millimeters to 5 cm in diameter. Contrast-enhanced MDCT is
very helpful in the noninvasive evaluation of the bronchial
and systemic circulation, including BAA, given its high spa-
tial and contrast resolution and multiplanar capability with
3-dimensional reconstruction (Fig. 22).36,84-86 Cardiac-gated
CT reduces motion artifact and allows better delineation of
the bronchial circulation and detection of BAA.87

Pulmonary Venous Aneurysms

Pulmonary vein aneurysms can present as an isolated finding
or in association with other cardiopulmonary diseases. A lo-
calized aneurysmal dilatation of a pulmonary vein, also re-

Figure 23 Pulmonary arteriovenous aneurysm in a patient with he-

reditary hemorrhagic telangiectasia. (A) Right pulmonary artery
catheter angiography shows the malformation with dilated vessels
and an aneurysmal sac (arrow). (B) Selective injection of the feeding
artery better depicts the arteriovenous aneurysm with dilated artery
and vein.

ferred to as a pulmonary varix in the literature, can be an

Figure 22 Rasmussen aneurysm of the left upper lobe in a patient with
history of TB and a new episode of hemoptysis. Left upper lobe cavity
culture was positive for Aspegillus niger. (A) Contrast-enhanced CT
shows a mural aneurysm in the wall of a left upper lobe cavity (arrow).
(B) Selective bronchial artery angiography demonstrates the irregular
aneurysm arising from the systemic bronchial circulation (arrow).
incidental finding in healthy individuals or be associated
with conditions like pulmonary venous hypertension, mitral
regurgitation, acquired and congenital heart disease, and
anomalous pulmonary venous return. They have been re-
ported also in association with numerous syndromes (eg,
Klippel–Trenaunay–Weber syndrome and Turner syn-
drome).88-93
Probably, more common is the presence of a pulmonary
vein aneurysm secondary to an AVM of the lung. Aneurysms
564
associated with AVM may involve both the arterial and ve-
nous side of the vascular anomaly, but when massive dilation
occurs, more often the venous side is dilated. Pulmonary
AVM may be congenital or acquired (trauma, infection, cir-
rhosis, surgery), but more than 80% are congenital, and out
of these, half or more are associated with hereditary hemor-
rhagic telangiectasia (HHT or Osler–Weber–Rendu dis-
ease).94,95 The anomaly contains a thin-walled fistula, and
despite being congenital, aneurysms are rarely discovered in
children. As the aneurysm expands, it becomes more evident
and usually diagnosed in the second or third decade of life. In
1965, Anabtawi et al96 proposed a classification of pulmo-
nary arteriovenous malformations based on the embryology
and morphology, which grouped them in 5 different catego-
ries. One of the morphological features considered for the
classification is the presence of arteriovenous aneurysm.
The classic radiographic presentation is that of a well-de-
fined round or oval mass, uniform in density, measuring
between 1 and 5 cm in diameter, in the periphery of the lung
(Fig. 23.). The draining pulmonary vein is invariably dilated,
and depending on the magnitude of the shunt, it can reach a
Figure 24 Right lower lobe arteriovenous malformation with venous
aneurysm. Contrast-enhanced CT. (A) Axial image at the level of the
right lower lobe pulmonary vein. (B) Axial image caudal to (A). The
images depict the abnormally dilated right lower lobe pulmonary
veins (arrows) with normal drainage into the left atrium.
C.S. Restrepo and A.P. Carswell
Figure 25 Large venous aneurysm in a 33-year-old female with he-
reditary hemorrhagic telangiectasia. Contrast-enhanced CT of the
chest shows the subpleural venous aneurysm (arrow) connected to
the left lower lobe pulmonary vein.
significant diameter (Fig. 24). The majority of venous aneu-
rysms are relatively modest in size but giant aneurysms, 6-10
cm in diameter, may occur (Fig. 25). When located on the
medial aspect of the lung, they may present on imaging ex-
aminations as a vascular mediastinal mass.97-99 Even though
noncontrast CT can demonstrate pulmonary arteriovenous
malformation, contrast-enhanced CT and magnetic reso-
nance imaging better depict the vascular nature, the anat-
omy, and angioarchitecture of the anomalies.100-103
Conclusions
Although uncommon, pulmonary aneurysms and pseudoa-
neurysms are important vascular abnormalities with signifi-
cant morbidity and mortality and often reflect the presence of
a serious underlying medical condition. Catheter angiogra-
phy has been largely replaced by noninvasive cross-sectional
imaging in the examination of pulmonary vascular diseases.
MDCT in particular plays an important role in detecting and
characterizing the different types of aneurysms of the bron-
chopulmonary vasculature. MDCT also provides useful in-
formation for treatment planning in patients with hemopty-
sis, which is a common clinical manifestation of these
conditions, and allows noninvasive follow-up after treat-
ment.
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